It is clear that although active sleep may appear to be a relatively quiescent behavioral state that is dependent upon potent patterns of postsynaptic inhibition of motoneurons, muscles do contract sporadically The underlying motor control landscape of active sleep is therefore one ravished not only by continuous storms of inhibitions, but also by brief whirlwinds of excitation that are directed toward "the final common pathway," the somatic motoneuron. thus, from the perspective of somatic motoneurons, active sleep is an exceptionally "active" state. In the present application we propose to explore the active sleep (as well as during quiet sleep). In the pursuit of this objective, the intracellular activity of lumbar motoneurons will be recorded in conjunction with the juxtacellular microiontophoretic ejection of excitatory amino acid agonists and antagonists in chronic undrugged, unanesthetized cats during spontaneously occurring behavioral states. A series of intracellular microiontophoretic studies will be undertaken. The specific aims are to determine the neurotransmitter(s) which are responsible for the EPSP activity and subsequent discharge of flexor and extensor lumbar motoneurons during the non-REM and REM periods of active sleep. Juxtacellular microiontophoretic studies will also be undertaken of the neurotransmitters involved with the PGO-related postsynaptic excitation of flexor and extensor lumbar motoneurons during the preceding states. The data from the proposed experiments will complement our previous examination of the inhibitory neurotransmitters that control the suppression of motoneuron activity during quiet and active sleep by determining the neurotransmitter(s) that mediate the excitatory processes that occur independent of, as well as in conjunction with, the inhibition of motoneurons.